Erratum: RIP1 Kinase Drives Macrophage-Mediated Adaptive Immune Tolerance in Pancreatic Cancer (Cancer Cell (2018) 34(5) (757–774.e7), (S1535610818304720), (10.1016/j.ccell.2018.10.006))

Wei Wang, Jill M. Marinis, Allison M. Beal, Shivraj Savadkar, Yue Wu, Mohammed Khan, Pardeep S. Taunk, Nan Wu, Wenyu Su, Jingjing Wu, Aarif Ahsan, Emma Kurz, Ting Chen, Inedouye Yaboh, Fei Li, Johana Gutierrez, Brian Diskin, Mautin Hundeyin, Michael Reilly, John D. LichPhilip A. Harris, Mukesh K. Mahajan, James H. Thorpe, Pamela Nassau, Julie E. Mosley, Joshua Leinwand, Juan A. Kochen Rossi, Ankita Mishra, Berk Aykut, Michael Glacken, Atsuo Ochi, Narendra Verma, Jacqueline I. Kim, Varshini Vasudevaraja, Dennis Adeegbe, Christina Almonte, Ece Bagdatlioglu, Deirdre J. Cohen, Kwok Kin Wong, John Bertin, George Miller

Research output: Contribution to journalComment/debate

6 Scopus citations

Abstract

(Cancer Cell 34, 757–774.e1–e7; November 12, 2018) We reported that RIP1 kinase signaling in macrophages promotes suppression of anti-tumor immunity in pancreatic cancer. During preparation of the manuscript, we submitted an incorrect version of Figure 1H in which one slide from the 3 month “RIP1i” group was inadvertently omitted from the analysis in the bar graph. We have included here a corrected version of Figure 1. In the original article, the legend for Figure 1H incorrectly states n = 8. The correct n values are n = 6 for control groups, n = 7 for RIP1i 3 months, and n = 8 for RIP1i 6 months. Similarly, in the originally published version of Figure 4K we inadvertently omitted one value for TNFα and MHC II. We have included here a corrected version of Figure 4. In the original version of the Figure 5C legend, the n values in the figure legend needed to be corrected to read as follows: n = 10 for Control (Tbet+) and RIP1i (TNFα+); n = 9 for Control (IFNγ+, TNFα+, IL-17+, RORγt+) and RIP1i (Tbet+, RORγt+); n = 8 for RIP1i (IFNγ+); and n = 7 for RIP1i (IL-17+). We excluded from the analysis flow cytometry tubes with fewer than 1,000 viable cells. Similarly, in the originally published article, the Figure 7A legend incorrectly stated that n = 9, when there are only 8 data points for the HLA-DR+ Control group, 5 data points for the IL-10+ Control group, 8 data points for the HLA-DR+ RIP1i group, and 5 data points for the IL-10+ RIP1i group. In the originally published Figure 8A, the n value listed in the legend was not accurate for select groups. Here we have included a corrected version of Figure 8 containing a dot plot for Figure 8A that depicts the correct n value (TNFα: n = 3 in vehicle, n = 6 in STAT1i, n = 2 in RIP1i, and n = 6 in STAT1i+RIP1i group; IFN-γ: n = 2 in vehicle, n = 5 in STAT1i, n = 2 in RIP1i, and n = 6 in STAT1i+RIP1i group; MHC-II: n = 4 in vehicle, n = 6 in STAT1i, n = 5 in RIP1i, and n = 5 in STAT1i+RIP1i group; IL-10: n = 6 in vehicle, n = 6 in STAT1i, n = 5 in RIP1i, and n = 3 in STAT1i+RIP1i group). The originally published Figure 8H legend incorrectly stated that the experiment was performed in replicates of five. There are actually 12 data points in the Control group, 6 data points in the PPARγi+ group, 12 data points in the RIP1i+ group, and 4 data points in the RIP1i+ PPARγi+ group. Note that 2 data points were excluded from the PPARγi+ RIP1i+ group as a result of a pipetting error. These errors do not affect any of the conclusions in the article, and we apologize for any confusion these errors may have caused. Below please see corrected versions of Figures 1, 4, and 8 and corrected figure legends for Figures 1, 5, 7, and 8. [Figure presented] [Figure presented] Figure 5. RIP1 Regulates Macrophage Differentiation and Immunogenicity (A) Expression of MHC-II, TNFα, IFN-γ, CD206, IL-10, and TGF-β in day-7 BMDM treated with RIP1i or vehicle for 18 hr. This experiment was performed more than five times in replicates of five. (B) Expression of surface activation markers in Ova-restricted CD4+ T cells co-cultured for 96 hr with TAMs harvested from day-21 PDA tumors of mice treated with RIP1i or control chow and pulsed with Ova323–339 peptide. This experiment was performed four times in replicates of five. (C) Expression of cytokines and transcription factors in Ova-restricted CD4+ T cells co-cultured for 96 hr with TAMs harvested from day-21 PDA tumors of mice treated with RIP1i or control chow and pulsed with Ova323–339 peptide (n = 10 for Control (Tbet+) and RIP1i (TNFα+); n = 9 for Control (IFNγ+, TNFα+, IL-17+, RORγt+) and RIP1i (Tbet+, RORγt+); n = 8 for RIP1i (IFNγ+); and n = 7 for RIP1i (IL-17+)). This experiment was performed four times. (D and E) Expression of surface activation markers (D) and cytokines and transcription factors (E) in Ova-restricted CD8+ T cells co-cultured for 96 hr with TAMs harvested from day-21 PDA tumors of mice treated with RIP1i or control chow and pulsed with Ova257–263 peptide. This experiment was performed twice in replicates of five. (F and G) Expression of CD44 (F) and LFA1 (G) in Ova-restricted CD4+ T cells co-cultured for 96 hr with BMDM treated with RIP1i or vehicle plus a neutralizing α-TNFα mAb or isotype and pulsed with Ova323–339 peptide. This experiment was performed twice in replicates of five. (H and I) Expression of CD44 (H) and LFA1 (I) in Ova-restricted CD8+ T cells co-cultured for 96 hr with BMDM treated with RIP1i or vehicle plus a neutralizing α-TNFα mAb or isotype and pulsed with Ova257–264 peptide. This experiment was performed twice in replicates of five. Data are displayed as average ± SEM (p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001). See also Figure S4. Figure 7. Inhibition of RIP1 in Organotypic Models of Human PDA Activates Innate and Adaptive Immunity and Decreases Tumor Viability (A) Select contour plots and quantification of the expression of HLA-DR, IFN-γ, TNFα, and IL-10 in PBMC-derived monocytes treated with RIP1i or vehicle (HLA-DR: n = 8 in both Control and RIP1i groups; IFN-γ and TNFα: n = 9 in both Control and RIP1i groups; IL-10: n = 5 in both Control and RIP1i groups). (B and C) Tumor cell viability (B) and the relative sizes of spheroids (C) of PDOTS (n = 5 patient samples) treated with RIP1i or vehicle. (D) The relative levels of indicated inflammatory mediators in supernatant of PDOTS from PDA patients (n = 5) treated with RIP1i versus vehicle. (E and F) Expression of HLA-DR, IFN-γ, and IL-10 in TAMs (E) and expression of IFN-γ, CD25, and CD69 in CD4+ T cells (F) from PDOTS (n = 10) treated with RIP1i or vehicle. Representative contour plots and quantitative data are shown as fold change compared with vehicle treatment. (G–I) Expression of CD25 (G), IFN-γ (H), and CD69 (I) in CD4+ T cells from PDOTS (n = 6 patients) treated with vehicle, RIP1i alone, αPD-1 alone, or RIP1i + αPD-1. Representative contour plots and quantitative data are shown as fold change compared with vehicle treatment. Data are displayed as average ± SEM (p < 0.05; ∗∗p < 0.01; ∗∗∗∗p < 0.0001).

Original languageEnglish
Pages (from-to)585-590
Number of pages6
JournalCancer Cell
Volume38
Issue number4
DOIs
StatePublished - Oct 12 2020

Bibliographical note

Publisher Copyright:
© 2020 Elsevier Inc.

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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